Myopia is the most common type of refractive errors characterized by excessive elongation of the ocular globe. With the increasing prevalence of myopia, improved knowledge of factors involved in myopia development is of particular importance. There are growing evidence suggesting that the choroid plays an important role in the regulation of eye growth and the development of myopia. Studies have demonstrated that thinning choroid is a structural feature of myopia, with a negative correlation between choroidal thickness and axial length, suggesting that the change in choroidal thickness may be a predictive biomarker for long‐term changes in ocular elongation. Given the fact that the choroid is primarily a vascular structure capable of rapidly changing blood flow, variations of choroidal thickness might be primarily caused by changes in choroidal blood flow. Considering that hypoxia is associated with myopia and choroidal blood flow is the main source of oxygen and nourishment supply, apart from the effect on myopia possibly by changing choroidal thickness, decreasing choroidal blood flow may contribute to scleral ischaemia and hypoxia, resulting in alterations in the scleral structure and thus leading to myopia. This review aims to provide an overview of recent work exploring the influence of the choroid on myopia from perspectives of choroidal thickness and blood flow, which may present new predictive indicators for the onset of myopia and new targets for the development of novel therapeutic approaches for myopia.

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DNA methyltransferases (DNMTs) 1, 3a, and 3b affect DNA promoter methylation; studies have suggested that they have important roles in the development of cancers. In this study, we analyzed the expression of DNMTs 1, 3a, and 3b; the MIB-1 labeling index; and their clinical significance in 6 normal retinas and 62 retinoblastomas using immunohistochemical analysis. We found that DNMT proteins were not expressed in normal retinas, whereas they were frequently expressed in retinoblastomas (DNMT1, 100%; DNMT3a, 98%; and DNMT3b, 92%). Compared with well-differentiated retinoblastomas, the expression of DNMTs 1 and 3a significantly increased in poorly differentiated retinoblastomas (P = .002 and P = .003, respectively); in addition, the frequency of their increased expression was high. DNMT1 expression was significantly higher in invasive retinoblastoma. Furthermore, the expression of DNMTs was positively correlated with the MIB-1 labeling index in retinoblastoma. Our findings suggest that the overexpression of DNMTs 1, 3a, and 3b may be related to retinoblastoma tumorigenesis and progression and may represent a novel approach for retinoblastoma therapy.

Our case involves a 19-year-old patient with forme fruste keratoconus. Small-incision lenticule extraction was performed, and 6.5 months after surgery, corneal ectasia was diagnosed. Preoperatively, the minimum central corneal thickness was 546 μm in the right eye and 542 μm in the left eye; the refractive correction was -6.75 -1.00 × 45 and -6.75 -0.75 × 140, respectively; the lenticular thickness was 137 μm and 135 μm, respectively. At 6.5 months, ectasia was diagnosed based on anterior and posterior surface keratometry of 38.4/39.5 diopters (D) and -6.3/-6.8 D, respectively, in the right eye and 38.6/40.8 D and -7.1/-6.6 D, respectively, in the left eye. The keratometry increased gradually and the corneal thickness decreased after surgery, and these trends continued during the 13-month follow-up. This report documents corneal ectasia as a complication of small-incision lenticule extraction and highlights the importance of preoperative evaluation and the need for long-term follow-up.

To perform safe and successful corneal refractive surgery on myopic patients, corneal thickness (CT) and corneal epithelial thickness (CET) must be accurately measured. Numerous individuals with myopia wear soft contact lenses (SCLs) for the correction of visual acuity but may subsequently undergo corneal refractive surgery. The aim of the present study was therefore to investigate the effects of long-term SCL wear on the CT and the CET of myopic subjects in order to guarantee the safety and accuracy of subsequent corneal refractive surgeries. Fifty-six subjects prepared to receive refractive surgery at Jinan Mingshui Eye Hospital (Zhangqiu, China) from April to July 2013 were included in the study. CT and CET were measured in subjects immediately following discontinued SCL wear (group I, 56 eyes), and subsequently following >two weeks of discontinued SCL wear (group II, 56 eyes). Ninety-four subjects with no history of corneal contact lens wear were enrolled as a control group. The CT and CET were measured at positions with a radius of 0.0‑1.0, 1.0-2.5 (divided into eight quadrants) and 2.5-3.0 mm (divided into eight quadrants) away from the corneal center using the RTVue-100 Fourier-domain anterior segment optical coherence tomography system. A significant decrease in the CT of the subjects in group II was observed, compared with that of group I and the control group (P<0.05). A significant decrease was observed in the CET of groups I and II compared with that of the control group (P<0.05). Following discontinuation of SCL wear, CET increased. However, the increased CET was unable to reach the normal range exhibited by the control group. Edema and thinning of the corneal stroma, as well as thinning of the corneal epithelium were observed in groups I and II. In conclusion, it was proposed that in clinical practice, for myopic patients following long-term SCL wear, CT and CET should be determined ≥ two weeks following discontinuation of SCL wear, once a stable CT and CET are obtained.

Riboflavin/UVA cross-linking is a technique introduced in the past decades for the treatment of keratoconus, keratectasia, and infectious keratitis. Its efficacy and safety have been investigated with clinical and laboratory studies since its first clinical application by Wollensak for the treatment of keratoconus. Although its complications are encountered during clinical practice, such as infection inducing risk, minimal invasion merits a further investigation on its future application in clinical practice. Recently, collagen cross-linking in sclera shows a promising prospect. In present study, we summarized the representative studies describing the clinical and laboratory application of collagen cross-linking published in past decades and provided our opinion on the positive and negative results of cross-linking in the treatment of ophthalmic disorders.

Background: Des-γ-carboxy prothrombin (DCP) is a serum protein produced by hepatocellular carcinoma (HCC) cells in the absence of vitamin K. Serum and tissue DCP expressions are thought to reflect the biological malignant potential of HCC. Hence, we aimed to examine the efficacy of vitamin K₂ on the production of DCP as well as tumor cell growth and invasion. Methods: Cell growth and viability were evaluated by 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide assay. The in vivo efficacy of vitamin K₂ was examined in nude mice bearing HCC cells. A 24-well transwell chamber was used to evaluate the motility and invasive ability of HCC cells. Levels of DCP in supernatant of cultures and in serum of mice were measured using an electrochemiluminescence immunoassay method. Western blot and immunohistochemical analysis were employed to evaluate the expression of DCP in HCC. Results: Vitamin K₂ (2–40 μM) significantly decreased the levels of DCP production in supernatant of PLC/PRF/5 and HepG2 cells and in serum of nude mice bearing HCC xenografts. The inhibition of DCP was also observed using the assays of Western blot analysis in HCC cultures and immunohistochemical analysis in HCC xenografts in mice. As a result of administration of vitamin K₂, the capacity of HCC growth was inhibited and the invasion and migration of tumor cells were decreased. Furthermore, the inhibitory effects of HCC growth were also observed in vivo and the sensitivitywas well correlated with the decrease of DCP in the serum of mice. Conclusion: Vitamin K₂ might suppress the growth and invasion of HCC cells via decrease of DCP.